Renal Flashcards
(64 cards)
Hydronephrosis
Urine back pressure into calyces compresses the nephrons within the medullary pyramids
- can lead to renal failure
- kidneys are enlarged and palpable
Treat causes:
Upper tract:
- Acute: insertion of a nephrostomy tube
- Chronic: insertion of a ureteric stent or a pyeloplasty
Lower tract: insertion of a urinary catheter or a suprapubic catheter
Pyelonephritis
Pyelonephritis is a kidney infection that occurs when bacteria from a urinary tract infection spreads to the kidney.
Amoxicillin (IV) + Gentamicin (IV)
Penicillin allergic: Switch Amoxicillin with Co-trimaxazole (IV)
Step down to: Co-trimaxazole (IV)
Chronic Kidney Disease
- reduced GFR
Stage 1: GFR >90 + evidence of kidney damage
Stage 2: GFR 60-90 + evidence of kidney damage
Stage 3: GFR 30-60
Stage 4: GFR 15-30
Stage 5: <15 or on RRT
Slow progression and reduce cardio risk:
- Reduce BP (ACEis/ ARBs)
- Statins
- Stop smoking
Nephrotic Syndrome
Non-proliferative process affecting podocytes
Symptoms: Oedema
Increased protein in the urine and decreased protein (albumin) in the blood, with increased fat in the blood.
Fluid restriction Salt restriction ACEi/ ARBs Anticoagulants IV Albumin
Glomerulonephritis
Immune mediated disease of the kidneys affecting glomeruli
Non-proliferative: Minimal change, FSGS, Membranous
- can cause Nephrotic syndrome
Proliferative: IgA, Rapidly progressive, post-infective
- can cause Nephritis syndrome
All GNs: Dietary changes Stop smoking ACEs/ARBs Statins
Treat underlying type
Severe: RRT
Minimal change GN
Non-proliferative
Nephrotic
- Oedema
- Proteinuria
- Decrease in blood protein
- Increase in blood lipids
Corticosteroids
Does not lead to CKD
Minimal change GN
Non-proliferative
Nephrotic
- Oedema
- Proteinuria
- Decrease in blood protein
- Increase in blood lipids
Corticosteroids
Cyclophosphamide
Does not lead to CKD
Focal segmental glomerulosclerosis (FSGN)
Non-proliferative
Nephrotic
Characterised by a sclerosis of segments of some glomerules, associated with conditions such as HIV and heroin abuse, or inherited as Alport syndrome.
Increase in hyalin and lipids. Low albumin.
Corticosteroids
Leads to CKD
Membranous (MGN)
Non-proliferative
Nephrotic/ nephritic
Associated with auto-antibodies to phospholipase A2 receptor, cancer, Hep B/c, Malaria, Syphilis, and SLE.
Corticosteroids
1/3 lead to CKD
IgA Nephropathy GN
Proliferative
Nephritic
The most common type of glomerulonephritis
- several days after a respiratory infection
- characterised by deposits of IgA in the space between glomerular capillaries
- Haematuria
- Low grade proteinuria
Self resolving
Omega 3 oil
Leads to CKD
Henoch–Schönlein purpura
A form of IgA nephropathy, typically affecting children, characterised by a rash of small bruises affecting the buttocks and lower legs, with joint pain and abdominal pain
Analgesia
Self sesolving
Post-infectious GN
Proliferative
Nephritic
Classically occurs after infection with the bacteria Streptococcus pyogenes. 1–4 weeks after a pharyngeal infection.
Presents with malaise, a slight fever, nausea and increased blood pressure, gross haematuria, and smoky-brown urine
Steroids
Rapidly progressive (PRGN)
Proliferative
Nephritis
Characterised by a rapid, progressive deterioration in kidney function.
Type 1: Goodpastures syndrome. IgG antibodies directed against the glomerular basement membrane trigger an inflammatory reaction. Haemoptysis.
Type 2: immune-complex-mediated damage, and may be associated with systemic lupus erythematosus, post-infective glomerulonephritis, IgA nephropathy, and IgA vasculitis
Type 3: associated with causes of vascular inflammation including granulomatosis with polyangiitis (GPA) and microscopic polyangiitis. ANCA antibody.
Steroids
Cyclophasphamide, azathioprine, mycophenolate
Plasmaphoresis
Diabetic Nephropathy
Protein loss in the urine due to damage to the glomeruli may become severe, and cause a low serum albumin with resulting oedema resulting in nephrotic syndrome. GFR may progressively fall to less than 15.
Damage to the glomerular basement membrane allows proteins in the blood to leak through, leading to proteinuria. Deposition of abnormally large amounts of mesangial matrix causes periodic-acid schiff positive nodules called Kimmelstiel–Wilson nodules.
ACEis
Manage Diabetes
Leads to ESKD
- RRT
Ischaemic Nephropathy
Decrease in GFR and kidney perfusion.
Caused by: HTN, artherosclerosis, Vascular disease, fibromusclular dysplasia
Symptoms:
- Flash pulmonary oedema
- Abdominal bruits
- Artherosclerosis
ACEi
Angioplasty/ stent
Statin
Anti-platelets
Lupus Nephritis Class I
Minimal mesangial GN
Mesangial deposits are visible under an electron microscope
Hydroxychloroquine
KF rare
Lupus Nephritis Class II
Mesangial proliferative GN
Mesangial hypercellularity and matrix expansion. Microscopic haematuria with or without proteinuria may be seen.
Hydroxychloroquine
Corticosteroids
Tacrolimus
KF rare
Lupus Nephritis Class III
Focal glomerulonephritis
Indicated by sclerotic lesions involving less than 50% of the glomeruli.
Immunofluorescence reveals positively for IgG, IgA, IgM, C3, and C1q.
Haematuria and proteinuria are present.
Hydroxychloroquine
Corticosteroids
Acute: Cyclophosphamide / MMF (mycophenolate mofetil)
Chronic: Azathioprine/ MMF
KF rare
Lupus Nephritis Class IV
Diffuse proliferative nephritis
Most severe, and the most common subtype. More than 50% of glomeruli are involved.
Haematuria and proteinuria are present, frequently with nephrotic syndrome, hypertension, hypocomplementemia, elevated anti-dsDNA titres and elevated serum creatinine.
Hydroxychloroquine
Corticosteroids
Acute: Cyclophosphamide / MMF (mycophenolate mofetil)
Chronic: Azathioprine/ MMF
KF rare
Lupus Nephritis Class V
Membranous (MGN)
Diffuse thickening of the glomerular capillary wall and membrane thickening. Signs of nephrotic syndrome. Microscopic haematuria and hypertension.
Hydroxychloroquine
Corticosteroids
Cyclophosphamide + Tacrolimus/ MMF/ Azathioprine
KF rare
Lupus Nephritis Class VI
Advanced sclerosing lupus nephritis
Sclerosis involving more than 90% of glomeruli.
Hydroxychloroquine
Poor response to therapy.
They’re fucked.
Acute Kidney Injury
A decrease in urine output
Stage 1: <0.5 ml/kg/h for >6hrs
Stage 2: <0.5 ml/kg/h for >12hrs
Stage 3: <0.3 ml/kg/h for >24hrs, or 12hrs of anuria
Due to:
- blood vessel damage (vasculitis, renovascular diseases)
- glomerular disease
- interstitial injury (infection, TB, Sarcoid, SLE)
- tubular injury (ischaemia, rhabdomyolysis, gentamicin)
Fluid Resuscitation (0.9% crystalloid bolus, then repeat if necessary)
If low BP then use inotropes/ vasopressors
Treat underlying causes
RRT
Hyperkalaemia
Muscle weakness and abnormal heart rhythms
Normal: 3.5-5
Hyper: >5.5
Life threatening: >6.5
Protect myocardium: 10ml 10% calcium gluconate IV
Influx of K into cells: Insulin (Actrapid) with 50ml 50% dextrose Salbutamol Neb (90 mins)
Long-term: Calcium resonium (prevents absorption from GI tract)
Autosomal Dominant Polycystic Disease
Small, fluid-filled sacs called cysts to develop in the kidney
Symptoms:
- abdominal pain, HTN, haematuria, UTIs, kidney stones
HTN control
Tolvaptan
RRT
